Evidence map›Paper›PMID 31653854›Full record

ArticleNature communications2019

MT1-MMP directs force-producing proteolytic contacts that drive tumor cell invasion.

Robin Ferrari, Gaëlle Martin, Oya Tagit, Alan Guichard, Alessandra Cambi, Raphaël Voituriez, Stéphane Vassilopoulos, Philippe Chavrier

Abstract read
In one paragraph

Article in Nature communications, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 63 papers.

0numbers the graph read from it
0cells of the map it votes in
63citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

63 citing papers in PubMed.

  1. Review
  2. Review
  3. Review
  4. Article
  5. Article
  6. E-Cadherin Is a Structuring Component of Invadopodia in Pancreatic Cancer.Journal of cellular and molecular medicine · 2025
    Article
  7. Article
  8. Article
  9. Article
  10. The role and regulation of integrins in cell migration and invasion.Nature reviews. Molecular cell biology · 2025
    Review
  11. Review
  12. Review
  13. Review
  14. Review
  15. Article
  16. Cancer cell extravasation requiresBritish journal of cancer · 2024
    Observational
  17. Article
  18. Article
  19. Article
  20. Article

3 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

8 authors.

Robin FerrariSorbonne Université, Institut Curie, PSL Research University, CNRS, UMR 144, 26 rue d'Ulm, F-75005, Paris, France. robin.ferrari@curie.fr.
Gaëlle MartinInstitut Curie, PSL Research University, CNRS, UMR 144, 26 rue d'Ulm, F-75005, Paris, France.
Oya TagitDepartment of Tumor Immunology, Radboud Institute for Molecular Life Sciences, Radboud University Medical Center, Nijmegen and Oncode Institute, Nijmegen, The Netherlands.ORCID http://orcid.org/0000-0002-5773-6647
Alan GuichardInstitut Curie, PSL Research University, CNRS, UMR 144, 26 rue d'Ulm, F-75005, Paris, France.ORCID http://orcid.org/0000-0001-8623-9570
Alessandra CambiDepartment of Cell Biology, Radboud Institute for Molecular Life Sciences, Radboud University Medical Center, Nijmegen, The Netherlands.ORCID http://orcid.org/0000-0003-1597-1582
Raphaël VoituriezSorbonne Université, CNRS, UMR 8237, Jean Perrin Laboratory, Paris, France.
Stéphane VassilopoulosSorbonne Université, INSERM UMRS 974, Institute of Myology, Paris, France. s.vassilopoulos@institut-myologie.org.ORCID http://orcid.org/0000-0003-0172-330X
Philippe ChavrierInstitut Curie, PSL Research University, CNRS, UMR 144, 26 rue d'Ulm, F-75005, Paris, France. philippe.chavrier@curie.fr.ORCID http://orcid.org/0000-0002-7351-733X

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Unraveling the mechanisms that govern the formation and function of invadopodia is essential towards the prevention of cancer spread. Here, we characterize the ultrastructural organization, dynamics and mechanical properties of collagenotytic invadopodia forming at the interface between breast cancer cells and a physiologic fibrillary type I collagen matrix. Our study highlights an uncovered role for MT1-MMP in directing invadopodia assembly independent of its proteolytic activity. Electron microscopy analysis reveals a polymerized Arp2/3 actin network at the concave side of the curved invadopodia in association with the collagen fibers. Actin polymerization is shown to produce pushing forces that repel the confining matrix fibers, and requires MT1-MMP matrix-degradative activity to widen the matrix pores and generate the invasive pathway. A theoretical model is proposed whereby pushing forces result from actin assembly and frictional forces in the actin meshwork due to the curved geometry of the matrix fibers that counterbalance resisting forces by the collagen fibers.

Indexed as

Actin-Related Protein 2-3 ComplexActinsBreast NeoplasmsCell Line, TumorCollagen Type IExtracellular MatrixHumansMatrix Metalloproteinase 14Microscopy, ElectronModels, TheoreticalNeoplasm InvasivenessPodosomesPolymerizationProteolysisActin-Related Protein 2-3 ComplexActinsCollagen Type IMatrix Metalloproteinase 14

Identifiers

PMID31653854
PMCPMC6814785

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Registered trials

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.